Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a bi-ventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann, et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing”.
Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs. This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema is usually associated with relatively severe forms of heart failure and is often asymptomatic until the edema itself becomes severe, i.e. the patient is unaware of the pulmonary edema until it has progressed to a near fatal state when respiration suddenly becomes quite difficult.
In view of the potential severity of heart failure/pulmonary edema, it is highly desirable to detect the onset of these conditions within a patient and to track the progression thereof so that appropriate therapy can be provided. Many patients suffering heart failure/pulmonary edema already have pacemakers or ICDs implanted therein or are candidates for such devices. Accordingly, it is desirable to provide such devices with the capability to automatically detect and track heart failure/pulmonary edema.
Heretofore, a number of techniques have been developed for detecting heart failure and/or pulmonary edema using implantable cardiac devices based on analysis of a transthoracic impedance signal. In this regard, the presence of additional fluids in the lungs tends to lower the electrical impedance measured between electrodes implanted in the heart and the housing of the implanted device. Hence, a sustained decrease in transthoracic impedance is indicative of possible pulmonary edema/heart failure. See, for example, U.S. patent application Ser. No. 11/138,229, of Koh et al., filed May 25, 2005, entitled “System and Method for Impedance-Based Detection of Pulmonary Edema and Reduced Respiration Using an Implantable Medical System.” See, also, U.S. Pat. No. 5,876,353 to Riff, entitled “Impedance Monitor for Discerning Edema through Evaluation of Respiratory Rate”; U.S. Pat. No. 5,957,861 to Combs et al., entitled “Impedance Monitor for Discerning Edema through Evaluation of Respiratory Rate”; U.S. Pat. No. 6,512,949 also to Combs et al., entitled “Implantable Medical Device for Measuring Time Varying Physiologic Conditions Especially Edema and for Responding Thereto”; U.S. Pat. No. 6,473,640 to Erlebacher, entitled “Implantable Medical Device for Measuring Time Varying Physiologic Conditions Especially Edema and for Responding Thereto”; U.S. Pat. No. 6,595,927 to Pitts-Crick et al., entitled “Method and System for Diagnosing and Administering Therapy of Pulmonary Congestion”; U.S. Pat. No. 6,829,503 to Alt, entitled “Congestive Heart Failure Monitor”; and U.S. Patent Application 2004/0102712 of Belalcazar et al., entitled “Impedance Monitoring for Detecting Pulmonary Edema and Thoracic Congestion.”
It is also feasible to detect heart failure based on analysis of morphological features of the intracardiac electrogram (IEGM). The IEGM is a voltage signal measured using electrodes implanted within the heart that corresponds to cardiac electrical activity associated with the contraction of the various chambers of the heart. It has been found that a paced depolarization integral (PDI) derived from the IEGM generally decreases due to heart failure, apparently due to changes in the contractility and thickness of the heart wall caused by heart failure. (PDI is a well-known parameter derived from an integral of portions of the IEGM. For a description of PDI, also sometimes referred to as a depolarization gradient, see U.S. Pat. No. 4,759,366, to Callaghan.) It has also been found that the peak-to-peak amplitude of the QRS-complex of the IEGM tends to decrease due to heart failure. The QRS complex is an electrical signal associated with ventricular depolarization. Further, it is know that the maximum slope of the QRS-complex (referred to as Δmax or Dmax) tends to decrease due to heart failure.
Hence, it is feasible to configure a pacemaker to detect and analyze changes in IEGM morphology as well as changes in transthoracic impedance and generate an indication of possible heart failure and/or pulmonary edema. However, the present inventors have recognized that the effect of heart failure on IEGM morphology and transthoracic impedance depends, at least in part, on the type and severity of the heart failure, particularly whether heart failure is acute or chronic. Accordingly, it would be desirable to provide techniques for discriminating acute and chronic heart failure from one another and for generating appropriate warning signals and controlling therapy in response thereto. It is also desirable to warn of possible pulmonary edema. The present invention is generally directed to these ends.